Relation between the somatic  toxicity of dimethylnitrosamine and a genetically determined variation in the level and induction of cytochrome P450 in Drosophila melanogaster.
The insecticide-resistant Drosophila strain Hikone R differs genetically from sensitive strains by having a higher activity of cytochrome P450 and a lack of inducibility with phenobarbital. Toxicity tests with dimethylnitrosamine (DMN) showed that: (a) the toxic effect of DMN was higher in the insecticide-resistant strain than in sensitive strains in accord with data by Vogel (1980); and (b) induction with phenobarbital increased the toxicity of DMN in the sensitive strains but not in the resistant strain. A dominant gene, responsible for the metabolic pattern of Hikone R and the non-inducibility, was located to 66 cM, near the gene vg in chromosome 2. This gene is most likely identical with that causing insecticide resistance, described by Kikkawa (1961).
D000818:Animals; D003577:Cytochrome P-450 Enzyme System / Q000235:genetics*; D004128:Dimethylnitrosamine / Q000494:pharmacology*; D004331:Drosophila melanogaster / Q000235:genetics*; D004351:Drug Resistance; D004789:Enzyme Activation; D005799:Genes, Dominant; D014644:Genetic Variation; D008297:Male; D009152:Mutagenicity Tests; D009153:Mutagens; D010641:Phenotype
D009153:Mutagens; D003577:Cytochrome P-450 Enzyme System; D004128:Dimethylnitrosamine